Dissociation of thirst and sodium appetite in the furo/cap model of extracellular dehydration and a role for N-methyl-D-aspartate receptors in the sensitization of sodium appetite.

Hurley, Seth; Johnson, Alan Kim

doi:10.1037/a0034948

Cited by 12 publications

(36 citation statements)

References 40 publications

(63 reference statements)

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“…Effect of MK-801 on sodium appetite sensitization and mRNA expression in the LT. We previously found that administration of the NMDAR antagonist MK-801 prevented sodium appetite sensitization in the furo/cap model when sodium access was offered prior to water (22). One purpose of our studies was to extend the generalizability of this finding by using a water-first/sodium-second protocol.…”

Section: Subjectsmentioning

confidence: 80%

“…These effects result in a rapid onset of thirst and sodium appetite with a latency of ϳ1 h (17,31,50). Rats repeatedly treated with furo/cap reliably exhibit sensitization of sodium appetite when the order of water and sodium access is controlled by the experimenter (22). Specifically, when water is offered for 90 min before sodium access (the water-first/ sodium-second iteration of the furo/cap protocol) rats exhibit a progressive increase in sodium intake over successive furo/cap treatments.…”

mentioning

confidence: 97%

“…Structures of the LT also house components of the central RAAS, including the synthetic enzymes and precursors of ANG II and aldosterone, as well as receptors for both the steroid and peptide (24,25,41). When rats are repeatedly depleted of sodium, they display elevated sodium intake (10,14,22,39,43). Rats exhibit progressive (3,39,44) or rapid (19,22,43) increases in sodium intake after one to three episodes of sodium deficiency depending on the depletion protocol employed.…”

mentioning

confidence: 97%

“…Administration of central ANG II along with systemic aldosterone induces sensitization (43). Additionally, blockade of NMDARs prior to sodium depletion prevents sensitization of sodium appetite (22). It is likely that sodium depletion induces neuroplasticity in the central nervous system through the coordinated actions of ANG II, aldosterone, and glutamate, which are responsible for the elevation of sodium intake.…”

mentioning

confidence: 99%

“…When rats are repeatedly depleted of sodium, they display elevated sodium intake (10,14,22,39,43). Rats exhibit progressive (3,39,44) or rapid (19,22,43) increases in sodium intake after one to three episodes of sodium deficiency depending on the depletion protocol employed. This increase in salt intake operationally defines sodium appetite sensitization.…”

mentioning

confidence: 99%

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Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

Hurley

Zhang

Beltz

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Animals with a history of sodium depletions exhibit increases in salt intake, a phenomenon described as the sensitization of sodium appetite. Using a novel experimental design, the present experiments investigated whether putative molecular markers of neural plasticity and changes in the message for components of the brain renin-angiotensin-aldosterone-system (RAAS) accompany the sensitization of sodium appetite. An initial set of experiments examined whether the glutamatergic N-methyl-d-aspartate receptor antagonist MK-801 would attenuate sodium appetite sensitization and prevent changes in mRNA expression associated with sensitization. Rats with repeated sodium depletions exhibited enhanced sodium appetite and mRNA expression for components of the RAAS in areas along the lamina terminalis (LT), a region of the brain that is important for the regulation of body fluid homeostasis, and these effects were significantly attenuated by MK-801 pretreatment. A second set of experiments investigated whether successive sodium depletions would elevate sodium intake and induce a pattern of fos-B staining consistent with the Δfos-B isoform in areas along the LT. The pattern of fos-B staining in the subfornical organ was consistent with the characteristics of Δfos-B expression. Specifically, fos-B/Δfos-B expression was increased 4 days after the last of a series of sodium depletions, fos-B/Δfos-B expression was nearly absent in control rats, and the quantity of fos-B/Δfos-B staining was directly associated with a history of sodium depletions. These findings demonstrate that the sensitization of sodium appetite is associated with sustained molecular alterations in the LT that are indicative of neural plasticity and upregulation of the central RAAS.

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Section: Subjectsmentioning

confidence: 80%

mentioning

confidence: 97%

mentioning

confidence: 97%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

Hurley

Zhang

Beltz

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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The biopsychology of salt hunger and sodium deficiency

Hurley

Johnson

2015

Pflugers Arch - Eur J Physiol

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Sodium is a necessary dietary macromineral that tended to be sparsely distributed in mankind’s environment in the past. Evolutionary selection pressure shaped physiological mechanisms including hormonal systems and neural circuits that serve to promote sodium ingestion. Sodium deficiency triggers the activation of these hormonal systems and neural circuits to engage motivational processes that elicit a craving for salty substances and a state of reward when salty foods are consumed. Sodium deficiency also appears to be associated with aversive psychological states including anhedonia, impaired cognition, and fatigue. Under certain circumstances the psychological processes that promote salt intake can become powerful enough to cause “salt gluttony,” or salt intake far in excess of physiological need. The present review discusses three aspects of the biopsychology of salt hunger and sodium deficiency: 1) the psychological processes that promote salt intake during sodium deficiency, 2) the effects of sodium deficiency on mood and cognition, and 3) the sensitization of sodium appetite as a possible cause of salt gluttony.

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Short-term cross-sensitizion of need-free sugar intake by combining sodium depletion and hypertonic NaCl intake

et al. 2016

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History of sodium depletion cross-sensitizes the effects of drugs of abuse. The objective of the present study was to find out if history of sodium depletion also cross-sensitizes a natural reward such as sugar intake in the rat. Sodium depletion was induced by furosemide combined with removal of ambient sodium for 24 h; it was repeated seven days later. The depletion was immediately followed by 0.3 M NaCl intake in a sodium appetite test (active sodium repletion). Seven days after the last depletion, hydrated and fed (need-free) sucrose-naïve animals were offered 10% sucrose in a first 2-h sucrose test. The sucrose test was repeated once a day in a series of five consecutive days. History of sodium depletion enhanced sucrose intake in the first and second tests; it had no effect from the third to fifth sucrose test. The effect on the initial sucrose intake tests disappeared if the rats did not ingest 0.3 M NaCl in the sodium appetite test. Prior experience with sucrose intake in need-free conditions had no effect on sodium appetite. History of intracellular dehydration transiently influenced sucrose intake in the first sucrose test. We found no evidence for thirst sensitization. We conclude that history of dehydration, particularly that resulting from sodium depletion, combined to active sodium repletion, produced short-term cross-sensitization of sucrose intake in sucrose-naïve rats. The results suggest that the cross-sensitization of sucrose intake related with acquisition of sugar as a novel nutrient rather than production of lasting effects on sugar rewarding properties.

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Dissociation of thirst and sodium appetite in the furo/cap model of extracellular dehydration and a role for N-methyl-D-aspartate receptors in the sensitization of sodium appetite.

Cited by 12 publications

References 40 publications

Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

The biopsychology of salt hunger and sodium deficiency

Short-term cross-sensitizion of need-free sugar intake by combining sodium depletion and hypertonic NaCl intake

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